The present invention relates to a method for treating periodontal disease.
Periodontal disease is characterized by a loss of supporting tissues of the teeth. In particular, periodontitis includes a loss of the periodontal ligament and a disruption of the ligament attachments to cementum, as well as reabsorption of alveola and bone. Along with a loss of tissue attachments, periodontal disease produces a migration of the epithelial attachments along the root surface and reabsorption of bone.
It is widely accepted that an initiation and progression of periodontal disease is dependent upon the presence of micro-organisms which are capable of causing the disease. At least three characteristics of periodontal micro-organisms have been identified which contribute to the ability of microbes to act as pathogens. A first characteristic is a capacity of the microbes to colonize. A second characteristic is an ability of the microbes to evade anti-bacterial host defense mechanisms. A third characteristic is an ability of the microbes to produce substances which directly initiate tissue destruction.
Two major periodontal disease pathogens, A. actinomycetemcomitans and P. gingivalis, are able to invade into the tissues. A. actinomycetemcomitans passes through epithelial cells into the underlying connective tissue while P. gingivalis invades and persists in epithelial cells.
It is believed that direct pathological effects of bacteria and effects of their products on the periodontium are significant during early stages of periodontal disease. Analysis of plaque samples from patients with increasingly severe levels of gingival inflammation reveals a succession of bacterial species with an increased capacity to directly induce an inflammatory response. For example, an increase in persistent levels of Fusobacterium nucleatum incites a mild gingivitis. A subsequent production of its metabolic by-products directly effects gingival vasculature. Resulting edema and an increase in production of, gingival crevicular fluid, GCF, provides an environment and nutrients that allow putative pathogens to flourish.
Bacteria such as P. gingivalis also produce enzymes such as proviasis, collagenase, and fibrinolysin that directly degrade surrounding tissues in superficial layers of the periodontium. In addition, this bacterium produces metabolic by-products such as H2S, ammonia and fatty acids that are toxic to surrounding cells. Furthermore, bacterial constituents such as lipopolysaccharide are capable of inducing bone reabsorption in vitro.
Once major protective elements of the periodontium have been overwhelmed by bacterial virulence mechanisms, several host-mediated destructive processes are initiated. Polymorphonucleocytes (PMNS), which normally provide protection can themselves contribute to tissue pathology. During a process of phagocytosis, PMNs typically spill some of the enzyme content extracellularly during a process known as degranulation. Some of the enzymes are capable of degrading the surrounding host tissues, such as collagen and basement membrane constituents, which contribute to tissue damage.
There is increasing evidence that the bulk of tissue destruction in established dental lesions is a result of the mobilization of the host tissues by an activation of monocytes, lymphocytes, and other host cells. Engagement of these cellular elements by bacterial factors, in particular bacterial lipopolysaccharide, is thought to stimulate production of both catabolic cytokines and inflammatory mediators such as arachidonic acid and metabolites, such as prostaglandin E2 (PGE2). Such cytokines and inflammatory mediators, in turn, promote the release of tissue-derived enzymes. A summary of this reaction is described in an article, xe2x80x9cThe Pathogenesis of Periodontal Diseasesxe2x80x9d, Periodontal, April 1999, Vol. 70, No. 4, pp. 457-470.
In some aspects, periodontal diseases are among the most unusual infections of human beings. One reason for this uniqueness is the unusual anatomic feature wherein a mineralized structure, a tooth, passes through an integument so that a portion of the tooth is exposed to an external environment while a portion is within connected tissues. This unusual aspect of the infection is described in an article entitled xe2x80x9cThe Nature of Periodontal Diseasesxe2x80x9d by S. Socransky et al. in The Annals of Periodontology, vol.2, No. Mar. 1, 1997, pp. 4-10.
The tooth provides a surface for colonization by a diverse array of bacterial species. Bacteria attach to the tooth itself as well as to the epithelial surface of the gingival or periodontal pockets, and to underlying connective tissues. The outer layers of the tooth do not shed, and thus microbial colonization is facilitated. A situation is then established wherein micro-organisms colonize a relatively stable surface, which is the surface of the tooth, and are continually held in immediate proximity to soft tissues of the periodontium.
The presence of the tooth increases the complexity of the host-parasite relationship in a number of ways. The bacteria colonizing the tooth are by and large outside the body where they are less able to be controlled by mechanisms which operate within the tissues. The environment within a plaque is conducive to microbial survival, but it is unlikely to be particularly an effective environment for a host to seek out and destroy micro-organisms.
Factors such as pH, eH and proteolytic enzymes affect performance of host defense mechanisms. In addition, the tooth provides sanctuary in which micro-organisms hide, persist at low levels during treatment, and then re-emerge to cause further problems. Bacteria in dentin alluvials, which are flaws in the tooth, or areas which were demineralized by bacteria, are not easily approached by much larger host cells. In a similar manner, non-cellular host factors face diffusion barriers. Mechanical debridement, other than vigorous removal of tooth material, cannot reach organisms in the tooth. Chemotherapeutic agents also have difficulty in reaching the bacterial species. In particular, antimicrobial agents which require bacteria to multiply are adversely affected since the rate of growth is suspected to be very low.
One method for measuring the severity of periodontal disease is a technique of periodontal probing depth (PD). Measuring periodontal probing depth measures a loss of connective tissue attachments. A method of periodontal probing has been described in an article entitled xe2x80x9cPeriodontal Probing: Probe-tip Diameter*xe2x80x9d, published by the School of Dentistry, Medical College of Georgia, Augusta, Ga.
Periodontal probing is performed when a periodontist places a probe into the sulcus or clinical pocket, and applies a force to move it apically into tissue along a tooth surface. The clinician applies pressure on the tissue and when the tissue exerts an opposite, equal pressure to the probe, displacement of the probe into the tissue will cease. The pressure exerted by the probe is directly proportional to force on the probe and inversely proportional to the area at the probe tip. With a round probe, a change in the tip diameter has a greater effect on pressure than does a similar change in the force. An increase in the probing force increases the pressure by a proportional amount. However, a relatively similar increase of the probe diameter reduces the pressure by a proportional amount which is squared. If the force is doubled (20 to 40 gramforce), the pressure is increased by a factor of 2. If the diameter is doubled (0.4 to 0.8 millimeters), the pressure is reduced by a factor of 4. The pressure is equal to the force applied in the probe/area at the tip-end=F/ur2=F/u(D/2)2: R=radius, D=diameter.
Positioning of the probe is shown in schematic cross-section in FIG. 1. The probe 10 is inserted in an area between connective tissue 12 and dentin 14, as is shown in FIG. 1. The depth 16 of the probe 10 into that space is a measure of the severity of periodontal disease.
In early periodontitis, gums appear similar to those in gingivitis. However, the seal around a tooth has been destroyed and the bone is starting to eat itself away. This is an attempt by the body to escape advancing bacterial invasion. At this time, pockets are 4 to 5 millimeters deep.
In moderate periodontitis, the infection has eaten away more bone. Gums are receding, exposing root surfaces. Pus may be present. Pockets are up to about six millimeters deep. At this state of infection, the infection may still be treated non-surgically. However, once the bone is lost, it does not grow back. The teeth are weakened by partial loss of the supporting bone. In advanced periodontitis, bone loss becomes more severe. The gum tissue has now become more like scar tissue. The scar tissue must be cut out surgically to get ride of the pockets. Advanced periodontal pockets usually measure more than 6 millimeters.
Treatment regimens for periodontal disease typically involve removal of mechanical irritants, such as plague and calculus, and removal of as many bacteria as possible. The tissues are made as cleansable and as healthy as possible. The patient is taught to keep teeth and gums clean. Non-surgical treatment includes scaling and root cleaning, which is deep root cleaning of teeth to physically remove all tartar and plaque. The teeth are polished to remove stains and to make the teeth harder for the plaque to adhere to. Prescription and non-prescription medications are applied to the gums. Mouth rinses are used in conjunction with improved home care. Antibiotics are sometimes used.
Kakwarf et al., in an article entitled xe2x80x9cCytologic Evaluation of Gingival Curettage Facilitated by a Sodiumhypochloride Solutionxe2x80x9d, Internal Periodontology, February 1992, pp. 63-69, describes a use of an instrument against a gingival side of a pocket, in order to scrape and debride soft tissue. The purpose of this scraping and debriding is to remove inflamed tissue and to maintain teeth and gums in a state of periodontal health. In some treatments, sodium hypochlorite solution was introduced along with the curettage in order to remove all the epithelium from a pocket. Citric acid treatment has also been used to augment epithelial treatment.
Local controlled delivery of antibiotics has also been performed in conjunction with scaling and root cleaning. One antibiotic delivered through a controlled release mechanism is doxycycline hyclate. This type of treatment was described in an article written by Garret et al., entitled xe2x80x9cThe Effect of Locally-delivered Controlled Release Dioxycycline on Scaling and Root Cleaning on Periodontal Maintenance Patients over Nine Monthsxe2x80x9d, Periodontal Period, Vol. 71, No. 1 January 1, 2000, pp. 2-9. Other antibiotics delivered through this type of format include the tetracycline.
In cases of advanced periodontal disease, the gum adjacent to the diseased tooth is lifted from the tooth and bone, and diseased tissue is removed. The infected bone may also be reshaped. After surgery, the gum is repositioned and sutured into place.
In some cases, destroyed tissue between teeth or roots is partially regenerated. Once damaged area of tissue is removed and special membranes are inserted, new tissue grows over a period of weeks to months. This type of regeneration, as measured by a probe test, typically results in a decrease in probe depth of only about 1 millimeter.